ReportNEUROPROSTHETICS

Agonist-antagonist myoneural interface amputation preserves proprioceptive sensorimotor neurophysiology in lower limbs

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Science Translational Medicine  09 Dec 2020:
Vol. 12, Issue 573, eabc5926
DOI: 10.1126/scitranslmed.abc5926

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Preserving proprioception

Limb amputation disrupts sensorimotor signaling, impairing control of neuroprostheses. Srinivasan et al. mapped brain activation via functional magnetic resonance imaging in individuals with agonist-antagonist myoneural interface (AMI) amputation, individuals with traditional lower-limb amputation, and non-amputees. AMI amputation surgically creates autologous muscle-nerve interfaces. The authors found evidence of similar functional activation of the proprioceptive center of the brain, correlated to motor control and muscle activity, in individuals with AMI amputation and non-amputees, whereas individuals with traditional amputation showed reduced activation. Results help illustrate how AMI amputation preserves sensory feedback and motor control.

Abstract

The brain undergoes marked changes in function and functional connectivity after limb amputation. The agonist-antagonist myoneural interface (AMI) amputation is a procedure that restores physiological agonist-antagonist muscle relationships responsible for proprioceptive sensory feedback to enable greater motor control. We compared results from the functional neuroimaging of individuals (n = 29) with AMI amputation, traditional amputation, and no amputation. Individuals with traditional amputation demonstrated a significant decrease in proprioceptive activity, measured by activation of Brodmann area 3a, whereas functional activation in individuals with AMIs was not significantly different from controls with no amputation (P < 0.05). The degree of proprioceptive activity in the brain strongly correlated with fascicle activity in the peripheral muscles and performance on motor tasks (P < 0.05), supporting the mechanistic basis of the AMI procedure. These results suggest that surgical techniques designed to restore proprioceptive peripheral neuromuscular constructs result in desirable central sensorimotor plasticity.

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